E2 pellet

Manufactured by Innovative Research

Sourced in United States

E2 pellets are a laboratory product used for research purposes. They are small, compressed pellets made of a specific material. The core function of E2 pellets is to provide a standardized and controlled material for use in various scientific experiments and analyses. No further details can be provided while maintaining an unbiased and factual approach.

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Lab products found in correlation

Matrigel, by BD (2 mentions) Balb cj mice, by Jackson ImmunoResearch (1 mentions) Balb c nu nu mice, by Orient Bio (1 mentions) Saline 60 day slow release, by Innovative Research (1 mentions) Hydroxymethyl cellulose, by Merck Group (1 mentions) Phosphate buffered saline (pbs), by Thermo Fisher Scientific (1 mentions) Control pellets, by Innovative Research (1 mentions) Tamoxifen citrate, by Merck Group (1 mentions) Doxycycline, by Merck Group (1 mentions) Anti flag tag antibody, by Merck Group (1 mentions) 4 hydroxytamoxifen, by Merck Group (1 mentions) Nod scid mice, by Charles River Laboratories (1 mentions) Anastrozole, by Merck Group (1 mentions) Anti fibronectin, by Santa Cruz Biotechnology (1 mentions) Horse serum, by Thermo Fisher Scientific (1 mentions) Matrigel matrix growth factor reduced, by BD (1 mentions) Anti β actin, by Santa Cruz Biotechnology (1 mentions) Anti bcl 2, by Santa Cruz Biotechnology (1 mentions) Anti raf b, by Santa Cruz Biotechnology (1 mentions) Anti p21, by Santa Cruz Biotechnology (1 mentions)

23 protocols using e2 pellet

Ovariectomy and Carotid Artery Injury Model

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Ovariectomy was performed in anesthetized animals with 1% inhaled isoflurane at 8 to 12 weeks of age, as previously described.²¹ (link) One week later, a sustained-release E2 pellet (0.25 mg, 60-day release, Innovative Research of America) or placebo pellet was implanted subcutaneously.
The carotid artery wire injury was performed as previously described.¹⁴ (link) Briefly, the left common carotid artery of an anesthetized animal (1% to 2% inhaled isoflurane) was cannulated, and the endothelium was denuded by wire insertion through the external carotid artery. The right carotid artery of each mouse was subjected to a sham operation for the uninjured control in each mouse. On day 7 or 14, the mice were sacrificed, and the vessels were harvested.

Liu P.Y., Fukuma N., Hiroi Y., Kunita A., Tokiwa H., Ueda K., Kariya T., Numata G., Adachi Y., Tajima M., Toyoda M., Li Y., Noma K., Harada M., Toko H., Ushiku T., Kanai Y., Takimoto E., Liao J.K, & Komuro I. (2022). Tie2-Cre–Induced Inactivation of Non-Nuclear Estrogen Receptor-α Signaling Abrogates Estrogen Protection Against Vascular Injury. JACC: Basic to Translational Science, 8(1), 55-67.

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Orthotopic Breast Cancer Xenograft in SCID Mice

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All animal studies were conducted after obtaining UT Health San Antonio IACUC approval, and in accordance with IACUC guidelines. SCID mice (n = 5, per group) were implanted with E2 pellet (cat# SE-121, Innovative Research of America, Sarasota, FL) as described previously [35 (link)]. Model cells MCF7-Control, MCF7-SETDB1, MCF7-PELP1-KD, MCF7-PELP1-KD + SETDB1 (2 × 10⁶ cells) were mixed with equal volume of matrigel and injected orthotopically into the mammary fat pads of 8-week-old SCID mice. Tumor growth was measured using calipers at weekly intervals, and tumor volume was calculated using a modified ellipsoidal formula: tumor volume = 1/2(L × W²), where W is the transverse diameter and L represents longitudinal diameter. At the end of the experiment, mice were euthanized, and tumors were processed for histological studies.

Liu Z., Liu J., Ebrahimi B., Pratap U.P., He Y., Altwegg K.A., Tang W., Li X., Lai Z., Chen Y., Shen L., Sareddy G.R., Viswanadhapalli S., Tekmal R.R., Rao M.K, & Vadlamudi R.K. (2022). SETDB1 interactions with PELP1 contributes to breast cancer endocrine therapy resistance. Breast Cancer Research : BCR, 24, 26.

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Establishing Patient-Derived Xenograft Models

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Studies were approved by the Dartmouth College IACUC. Female NOD.Cg‐Prkdc^scidIl2rg^tm1Wjl/SzJ (NSG) mice (4–5 weeks old; obtained from the Norris Cotton Cancer Center Mouse Modeling Shared Resource) were ovariectomized and implanted subcutaneously (s.c.) with ~ 8‐mm³ fragments of serially transplanted WHIM16 patient‐derived xenograft (PDX) breast tumor tissue [obtained from the Washington University HAMLET Core (Puenpa et al., 2013)]. Female BALB/cJ mice (4–5 weeks old; obtained from Jackson Laboratory) were ovariectomized and implanted s.c. with fragments of serially transplanted C4‐HI or C7‐2‐HI murine mammary adenocarcinoma tissue [gifts from Claudia Lanari, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina (Kordon et al., 1991; Soldati et al., 2010; Vanzulli et al., 2005)]. In all mice, tumor volume was measured twice weekly using calipers (volume = width² × length/2). When tumors reached ~ 400 mm³, mice were randomized to receive sham surgery or s.c. implantation with an E2 pellet (0.72 mg, 60‐day release; Innovative Research of America, Sarasota, FL, USA). For molecular analyses, tumors were harvested at the indicated time points and cut into pieces for snap‐freezing.

Hosford S.R., Shee K., Wells J.D., Traphagen N.A., Fields J.L., Hampsch R.A., Kettenbach A.N., Demidenko E, & Miller T.W. (2019). Estrogen therapy induces an unfolded protein response to drive cell death in ER+ breast cancer. Molecular Oncology, 13(8), 1778-1794.

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Rottlerin Inhibits Ishikawa Cell-Derived Xenograft Tumors

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Approximately 5-week-old female Balb Cnu/nu mice were purchased from Orientbio Inc. (Seongnam, Korea). Mice were maintained as previously described [42 (link)]. An E₂ pellet (1.7 mg/60-day release; Innovative Research of America) was implanted subcutaneously before the injection of Ishikawa cells. Five days later, Ishikawa cells (1.5×10⁷) in 100 μL of DMEM/F12:Matrigel (1:1) were subcutaneously injected into the dorsal flank of each mouse. Two days later, 5 mg/kg of rottlerin in DMSO was administered intraperitoneally to the mice daily for 22 days, and the control mice were given DMSO in the same manner. Tumor volumes and body weights of mice were measured at every 3 days. Tumors were measured with Vernier calipers, and tumor volumes were calculated by the formula π/6×length×width×height. The mice were sacrificed under anesthesia, and the tumors were collected for further analysis.

Koo K.H., Jeong W.J., Cho Y.H., Park J.C., Min D.S, & Choi K.Y. (2015). K-Ras stabilization by estrogen via PKCδ is involved in endometrial tumorigenesis. Oncotarget, 6(25), 21328-21340.

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Estradiol Replacement in ArKO Mice

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Male mice of both ArKO and WT at 3 and 6 months of age were used in these studies, groups included were: untreated WT, untreated ArKO and ArKO implanted 17β-estradiol pellet (E2). Three month-old ArKO mice were implanted with E2 pellet (E2) (0.05 mg in 21 days i.e. 2.5 µg/day, Innovative Research of America, Toledo, OH, USA) for 3 weeks. Six month-old ArKO mice were implanted with E2 pellet (0.15 mg in 60 days, i.e. 2.5 µg/day; Innovative Research of America, Toledo, OH, USA) 6 weeks. In preliminary studies no difference in body mass or glucose tolerance were detected between untreated and placebo pellet (saline 60 day slow release, Innovative Research of America, Toledo, OH, USA) treated six month-old ArKO male mice (Table S1 and Figure S1). A total number of 5–15 mice were used per group and age, details specified on related graphs. After treatment, mice were killed using a lethal dose of anesthetic (Ketamine (300 mg/kg)/Xylazine (30 mg/kg)). Blood was collected by cardiac puncture and serum was separated, and stored at −20°C. Adipose, liver and muscle tissues were removed, weighed, snap frozen and stored at −80°C.

Van Sinderen M.L., Steinberg G.R., Jørgensen S.B., To S.Q., Knower K.C., Clyne C.D., Honeyman J., Chow J.D., Herridge K.A., Jones M.E., Simpson E.R, & Boon W.C. (2014). Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse. PLoS ONE, 9(2), e87230.

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Evaluation of Fibroid Treatments in Mice

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The mice were anesthetized using 1.5% isoflurane (4% for induction) in an oxygen/nitrous oxide 30%/70% mixture. Dorsal incisions were made, bilateral oophorectomy was performed, and wounds were stapled. Animals were monitored carefully during the recovery phase and 5 mg Rimadyl/kg bodyweight was administered s.c. for pain relief. Three weeks after ovariectomy, the UF tissue pieces, were transplanted s.c. using a trocar. During the same surgery, mice were supplemented s.c. with (60 day release estrogen) E2 pellets (Innovative Research of America, Sarasota, FL, USA). Animals received EC313 0.1 mg/kg, N = 6, or 1 mg/kg, N = 6), or UPA (5 mg/kg, N = 5) by subcutaneous injection (s.c) for five days per week for 8.5 weeks. E2 control animals received E2 + vehicle (N = 5). 0.2% hydroxymethyl cellulose (Sigma Aldrich, St. Louis, MO) in phosphate buffered saline (Life technologies, Carlsbad, CA) was used as vehicle. At termination of the study animals were weighed, sacrificed, and the uterus and fibroid xenografts were excised and weighed. Tissues were harvested, fixed in 10% formalin, and processed for immunohistochemistry (IHC) for ER, PR, Ki67, desmin and α-SMA.

Nair H.B., Santhamma B., Dileep K.V., Binkley P., Acosta K., Zhang K.Y., Schenken R, & Nickisch K. (2019). EC313-a tissue selective SPRM reduces the growth and proliferation of uterine fibroids in a human uterine fibroid tissue xenograft model. Scientific Reports, 9, 17279.

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Ovariectomy-Induced Breast Cancer Xenograft Model

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Four-week-old female BALB/c (nu/nu) mice were obtained from Sun Yat-sen University. All animals were bred and housed at the Animal Experiment Center of Zhongshan School of Medicine, Sun Yat-sen University. The care and use of all animals followed the guidelines for laboratory animals, and the protocol was approved by Sun Yat-sen University Animal Policy and Welfare Committee. The mice were anaesthetized and underwent a bilateral ovariectomy (OVX) through a 1-cm dorsal incision. Meanwhile, E2 pellets (0.72 mg, 60-day release, Innovative Research) and control pellets (Innovative Research) were implanted subcutaneously. After surgery, the mice were allowed to recover for 1 week, and tumours were established by injecting MDA-MB-468 cells (5 × 10⁶ in 100 ml of Matrigel mixture) into the mammary fat pads of the mice. Callipers were used to measure the size of tumours every 5 days, and tumour volumes were calculated using the formula TV = length × [width] ² × 0.5. Forty-five days later, the mice were sacrificed, and the tumour specimens were harvested for further study.

Wang C., Li J., Ye S., Zhang Y., Li P., Wang L, & Wang T.H. (2018). Oestrogen Inhibits VEGF Expression And Angiogenesis In Triple-Negative Breast Cancer By Activating GPER-1. Journal of Cancer, 9(20), 3802-3811.

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Evaluating Tumor Growth in ER+ Breast Cancer

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For examination of the growth of tumors containing Wild Type ER, female NOD/SCID-gamma (NSG) mice were ovariectomized at 7–8 weeks of age, and 2 weeks after ovariectomy, animals were supplemented with 0.36 mg E2-pellets (60-day release, Innovative Research of America) to support ER+ tumor growth. Cell suspensions of wild type MCF7 cells (2 x 10⁶ cells/mouse) were injected orthotopically into the right axial mammary gland. When tumors reached 100–150 mm³ in size, mice were randomized and received compound or control vehicle (corn oil) by daily sc injection or oral gavage (PEG400/PVP/Tween/CMC as Veh) per day, for approximately 26 days, until Veh-treated tumors grew to ca. 1000 mm³. Tumor volume (length × width²/2) and animal body weights were monitored over time.
For examination of the growth of tumors containing mutant ERs, female NSG mice were ovariectomized but received no E2 pellets, to mimic the low estrogen environment of postmenopausal women. At 3 weeks after ovariectomy, cells were injected orthotopically into the axial mammary gland. Animals received daily sc injection or oral gavage of vehicle or compound, and tumor growth and animal body weights were monitored over time.

Zhao Y., Laws M.J., Guillen V.S., Ziegler Y., Min J., Sharma A., Kim S.H., Chu D., Park B.H., Oesterreich S., Mao C., Shapiro D.J., Nettles K.W., Katzenellenbogen J.A, & Katzenellenbogen B.S. (2017). Structurally novel antiestrogens elicit differential responses from constitutively active mutant estrogen receptors in breast cancer cells and tumors. Cancer research, 77(20), 5602-5613.

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BT474 Tumor Xenograft in Nude Mice

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Tumor xenograft studies were performed using the BT474 cell line in immunocompromised female mice based on previously reported protocols (27 (link), 28 (link)). We used 6-week-old BALB/c athymic, ovariectomized, nude female mice from Taconic Biosciences. After 1 week of acclimatization, we implanted subcutaneously 0.72 mg, 60-day release E2 pellets from Innovative Research of America to maintain a uniform level of estrogen. The next day we injected subcutaneously into both right and left flank of each mouse 2.5 × 10⁷ BT474 cells resuspended in 50% PBS and 50% Matrigel. Once all the animals harbored tumors of approximately 200 mm³, we randomized five animals to each treatment group. Half of the mice were implanted with vehicle pellets and the other half were implanted with 25 mg, 60-day release TAM pellets. We then randomized each group for vehicle or SXR injection. We performed biweekly injections (Monday and Friday) for 4 weeks. Each mouse was housed individually. Animals were monitored daily by the veterinarians for any signs of starvation, dehydration, stress, and pain. We monitored total weight, food intake, and tumor size using a digital caliper biweekly. Tumors were removed from euthenized mice at the end of the experiment or at the time when tumor size reached 1000 mm³ and then stored at −80°C for further analysis.

Wrobel K., Zhao Y.C., Kulkoyluoglu E., Chen K.L., Hieronymi K., Holloway J., Li S., Ray T., Ray P.S., Landesman Y., Lipka A.E., Smith R.L, & Madak-Erdogan Z. (2016). ERα-XPO1 Cross Talk Controls Tamoxifen Sensitivity in Tumors by Altering ERK5 Cellular Localization. Molecular Endocrinology, 30(10), 1029-1045.

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E2 Pellets and Tamoxifen for In Vivo and In Vitro Studies

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E2 pellets (0.36-mg 60-day release) for in vivo studies were purchased from Innovative Research (Sarasota, FL). Tamoxifen citrate (Tam) for in vivo studies and 4-hydroxy tamoxifen (Tam) and 17-beta estradiol (E2) for in vitro studies were purchased from Sigma (St Louis, MO). Doxycycline was purchased from Sigma (St Louis, MO). Antibodies against phosphorylated (p)H3, Ki67, and Cleaved Caspase 3–7 were obtained from Millipore (Billerica, MA), Dako (Carpinteria, CA), and Cell Signaling (Danvers, MA) respectively. Antibody against cJun was from Oncogene Research Products (La Jolla, CA). Anti- Flag Tag antibody was from Sigma (St Louis, MO).

Malorni L., Giuliano M., Migliaccio I., Wang T., Creighton C.J., Lupien M., Fu X., Hilsenbeck S.G., Healy N., De Angelis C., Mazumdar A., Trivedi M.V., Massarweh S., Gutierrez C., De Placido S., Jeselsohn R., Brown M., Brown P.H., Osborne C.K, & Schiff R. (2016). Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance. Molecular cancer research : MCR, 14(5), 470-481.

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